Word: amyloid
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...these genes, two - clusterin and CR1 - are known to interact with the amyloid protein that builds up in the brain of Alzheimer's patients and eventually causes nerve cell death and cognitive problems. Clusterin may be involved in helping to clear away the amyloid that forms in the brain; but another variant of the gene may also allow amyloid to form fibrils, the sticky protein arms that further anchor amyloid plaques to nerve cells, much like a spider web ensnares prey. In late-onset Alzheimer's, it's possible that the body cannot balance these two functions of clusterin...
...strategy was borne out in some of the conference's most exciting papers. Researchers from Mount Sinai School of Medicine reported, for example, that compared with other Alzheimer's patients, those who had diabetes and took insulin plus another anti-diabetes medication to control blood sugar had 80% fewer amyloid plaques - the sticky brain-clogging masses that, together with protein tangles, are the hallmarks of Alzheimer's disease. Although the mechanism wasn't entirely clear, researchers think the drugs may work by normalizing the brain's communication network of insulin receptors, which goes awry in the Alzheimer's brain, while...
Compared with patients who never developed diabetes, patients who had the disease but took insulin along with one additional medication to control blood sugar (typically metformin or glyburide) had 80% fewer brain-clogging amyloid plaques in their brain. Build up of these protein plaques, which are one of the hallmarks of Alzheimer's disease, can interfere with normal communication between nerve cells and cause deficits in memory and cognition. "The group on combination therapy had a very, very low load of neuritic plaques," Beeri says. "Their brains looked almost like normal people." The medications did not, however, do much...
...stems from genetics. There's a particular protein that's made in people with Alzheimer's - which is made from a protein that all of us make, the amyloid precursor protein. [In people with Alzheimer's] that precursor protein is clipped by enzymes in the wrong place, and begins to form these little toxic parts that aggregate [in the brain] and eventually form fibrils and plaques that are the main pathologic feature of Alzheimer's disease. It's not clear why this happens exactly, and a lot of people have been studying it pretty hard. It's also not clear...
...hundreds of companies working on treatments, that means relying on drug trials involving patients who may not even have the disease. "That's why the treatments we have now don't work that well," says Adams. In September, Amorfix announced that its technology can detect aggregated beta-amyloid, the protein fragment that, when gobbed together in the brain, is thought to identify Alzheimer's. With 460 million people worldwide over the age of 65, Adams estimates the market at as much as $5 billion...